非酒精性脂肪肝病(NAFLD)一线用药的空缺，使利用中医药宝库研究NAFLD新药和新靶点成为热点。前期研究表明3,4'-二甲氧基山奈酚(KP)具有成为抗NAFLD先导化合物的潜力，可与白细胞分化抗原36(CD36)结合抑制长链脂肪酸(LCFAs)摄入。同时KP可上调腺苷三磷酸结合盒转运蛋白A1(ABCA1)的磷酸化水平，但当沉默CD36基因后，则无此效应。故基于前期工作基础和国内外研究的最新进展，我们提出如下假说：KP通过与CD36结合抑制细胞对LCFAs的摄入，同时激活Src/PI3K/PKC/ABCA1通路促进细胞内LCFAs的外流，最终通过调控肝脏LCFAs的积累而干预NAFLD。本项目拟从分子、细胞和动物层面，利用光亲和标记探针、转录组学和组织特异性基因沉默等技术，阐明KP干预NAFLD的机制，论证CD36作为NAFLD新靶点的可能性，丰富中医药干预NAFLD的研究基础。

Nonalcoholic fatty liver disease (NAFLD) has became a worldwide public health problem. Because of no first-line medicines for the intervention of NAFLD, the researches about new drugs and targets of NAFLD have became hot topics. Previous researches indicated 3,4'-dimethoxykaempferol (KP), the active ingredient of Tamarix chinensis Lour., was a new leading compound of anti-NAFLD. KP could inhibite the combination of cluster of differentiation 36 (CD36) and long chain fatty acids (LFCAs) as a ligand of CD36. Meanwhile, KP could activate the phosphorylation of ATP Binding Cassette Subfamily A Member 1 (ABCA1). When the gene of CD36 were silenced, KP could not activate the phosphorylation of ABCA1. Therefore, based on the preliminary work and the current situation at home and abroad, we put forward the following hypothesis: KP might combine with CD36 to decrease LCFAs uptake, and activate the Src/PI3K/PKC/ABCA1 pathway to increase LCFAs outflow for the intervention of NAFLD by regulating the accumulation of LFCAs. This study intents to explore the mechanism of KP on NAFLD intervention from the molecule, cell and animal levels, and provide a new target and a new strategy for the intervention of NAFLD in traditional Chinese medicine.